A novel TLR3 inhibitor encoded by African swine fever virus (ASFV)

Oliveira, Victor De; Almeida, S. C. P.; Soares, Hugo R.; Crespo, Agustin Vega; Marshall‐Clarke, S.; Parkhouse, R. M. E.

doi:10.1007/s00705-010-0894-7

Cited by 85 publications

(77 citation statements)

References 31 publications

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“…In addition to activation of NF‐κB signaling in LPS‐treated cells, LPS also activates JAK/signal transducer and activator of transcription (STAT) signaling pathway [46, 47], and JAK/STAT signaling is important on chemokine expression [48, 49]. To investigate the relationship of JAK‐STAT signaling pathway on LPS‐induced chemokine expression, BV2 cells were pre‐treated with JAK/STAT inhibitor, AG490, for 30 min, and then stimulated with 1 μg/mL LPS for 12 hr.…”

Section: Resultsmentioning

confidence: 99%

Inhibitory effects of melatonin on the lipopolysaccharide‐induced CC chemokine expression in BV2 murine microglial cells are mediated by suppression of Akt‐induced NF‐κB and STAT/GAS activity

Min¹,

Jang²,

Kwon

2012

Journal of Pineal Research

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Melatonin influences sleep and circadian rhythm, and it has anti-inflammatory functions. However, the mechanism of its anti-inflammatory roles is not well understood. In our studies, we show that melatonin blocked lipopolysaccharide (LPS)-induced CCL2 (monocyte chemotactic protein-1; MCP-1), CCL5 (Regulated upon Activation, Normal T-cell Expressed, and Secreted), and CCL9 (macrophage inflammatory protein-1γ) chemokine mRNA expression in BV2 murine microglial cells. Melatonin markedly inhibited LPS-induced Akt phosphorylation and NF-κB activation. Furthermore, melatonin inhibited LPS-induced STAT1/3 phosphorylation and interferon-gamma activated sequence (GAS)-driven transcriptional activity. Interestingly, these effects were not associated with reactive oxygen species scavenging effects of melatonin or melatonin receptor signal pathways. Taken together, our results suggested that melatonin has anti-inflammatory functions through down-regulation of chemokine expression by inhibition of NF-κB and STAT/GAS activation in LPS-stimulated BV2 murine microglial cell line.

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Section: Resultsmentioning

confidence: 99%

Inhibitory effects of melatonin on the lipopolysaccharide‐induced CC chemokine expression in BV2 murine microglial cells are mediated by suppression of Akt‐induced NF‐κB and STAT/GAS activity

Min¹,

Jang²,

Kwon

2012

Journal of Pineal Research

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“…Three immune evasion genes (G protein-coupled receptor (GPCR), tumor necrosis factor receptor (TNFR), and Bcl-2 genes) from another iridovirus have been detected, and the results showed that the genes could regulate apoptosis in fish cells (Huang 2007). And what's more, recent research also revealed that many large double-stranded DNA viruses could encode an array of host evasion molecules that interfere with signaling cascades and anti-viral responses (Mohamed and McFadden 2009;FaganGarcia and Barry 2011;de Oliveira et al 2011). It is likely that RGV also contains immune evasion genes in its genome, which may facilitate virus invasion.…”

Section: Discussionmentioning

confidence: 99%

Characterization and virus susceptibility of a skin cell line from red-spotted grouper (Epinephelus akaara)

Chen

et al. 2012

Fish Physiol Biochem

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A red-spotted grouper Epinephelus akaara skin (RGS) cell line was established and characterized. RGS cells had a normal diploid chromosome number of 2n = 48, the morphology of which was fibroblastic-like in 3 days and epithelial-like over 5 after 16 passages. The cells multiplied well in Dulbecco's modified Eagle's medium supplemented with 10% of fetal bovine serum at 25°C. Susceptibilities of RGS and grass carp ovary (GCO) cells to two viruses were tested, and the results showed that the titer of an iridovirus Rana grylio virus (RGV) in RGS cells was 10 3.5 TCID 50 ml -1 , which was much higher than a rhabdovirus spring viremia of carp virus (SVCV) in the cells (10 0.5 TCID 50 ml -1 ). The titers of RGV and SVCV in GCO were 10 6.0 TCID 50 ml -1 and 10 8.0 TCID 50 ml -1 , respectively, which were higher than those in RGS cells. The data may imply that RGS cells could be selectively resistible to some viruses during infection. RT-PCR analysis of RGV-infected RGS cells showed that RGV could replicate in RGS cells. Further study of virus replications in RGS cells was conducted by electron microscopy and immunofluorescence microscopy has shown that virus particles scattered in the cytoplasm and virus protein appeared in both the cytoplasm and nucleus. The results suggested that RGS cells could be used as a potential in vitro model to study the cutaneous barrier function against virus infection.

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“…This latter effect seems specific to transcription factors that act through the N-terminal but not C-terminal domain of p300 (Granja et al, 2009). An ASFV Toll like receptor (TLR)3 inhibitor, encoded by the ASFV gene I329L has been identified (de Oliveira et al, 2011) which could reduce transcription of genes through its effect on the pattern recognition receptors (PPRs) and resultant downstream signalling pathways. In addition deletion of 6 members of multigene family 360 (MGF360) and 2 of multigene family 530 (MGF530), from a virulent isolate Pr4, was shown to result in an increased type I IFN response and induction of IFN stimulated genes (ISGs).…”

Section: Introductionmentioning

confidence: 99%

Modulation of chemokine and chemokine receptor expression following infection of porcine macrophages with African swine fever virus

Fishbourne¹,

Abrams²,

Takamatsu³

et al. 2013

Veterinary Microbiology

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African swine fever virus (ASFV) is the only member of the Asfarviridae, a large DNA virus family which replicates predominantly in the cytoplasm. Most isolates cause a fatal haemorrhagic disease in domestic pigs, although some low virulence isolates cause little or no mortality. The modulation of chemokine responses following infection of porcine macrophages with low and high virulence isolates was studied to indicate how this may be involved in the induction of pathogenesis and of effective immune responses. Infection with both low and high virulence isolates resulted in down-regulation of mRNA levels for chemokines CCL2, CCL3L, CXCL2 and chemokine receptors CCR1, CCR5, CXCR3, CXCR4 and up-regulation in expression of mRNAs for CCL4, CXCL10 and chemokine receptor CCR7. Levels of CCL4, CXCL8, CXCL10 mRNAs were higher in macrophages infected with low virulence isolate OURT88/3 compared to high virulence isolate Benin 97/1. Levels of CXCL8 and CCL2 protein were significantly reduced in supernatants from macrophages infected with Benin 97/1 isolate compared to OURT88/3 and mock-infected macrophages. There was also a decreased chemotactic response of donor cells exposed to supernatants from Benin 97/1 infected macrophages compared to those from OURT88/3 and mock-infected macrophages. The data show that infection of macrophages with the low virulence strain OURT88/3 induces higher expression of key inflammatory chemokines compared to infection with high virulence strain Benin 97/1. This may be important for the induction of effective protective immunity that has been observed in pigs immunised with the OURT88/3 isolate.

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A novel TLR3 inhibitor encoded by African swine fever virus (ASFV)

Cited by 85 publications

References 31 publications

Inhibitory effects of melatonin on the lipopolysaccharide‐induced CC chemokine expression in BV2 murine microglial cells are mediated by suppression of Akt‐induced NF‐κB and STAT/GAS activity

Inhibitory effects of melatonin on the lipopolysaccharide‐induced CC chemokine expression in BV2 murine microglial cells are mediated by suppression of Akt‐induced NF‐κB and STAT/GAS activity

Characterization and virus susceptibility of a skin cell line from red-spotted grouper (Epinephelus akaara)

Modulation of chemokine and chemokine receptor expression following infection of porcine macrophages with African swine fever virus

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